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Combined Exposure to Polystyrene Nanoplastics and Gentamicin Promotes Liver Toxicity Through Oxidative Stress, Inflammation and Apoptotic Pathways: In Vivo and In Silico Studies
Summary
Scientists found that when rats were exposed to tiny plastic particles (nanoplastics) together with a common antibiotic called gentamicin, their livers showed more damage than exposure to either one alone—including increased stress, inflammation, and cell death in liver tissue. This matters because it suggests that everyday exposure to plastic pollution might make certain medications more harmful to our organs, though more research is needed to confirm this happens in humans too.
Human exposure to nanoplastics and antibiotics is increasingly recognized as a major public health concern; however, the potential impacts of their combined exposure on human health remain poorly understood. In this study, we evaluated the hepatotoxic effects of polystyrene nanoplastics (PsNPs) and gentamicin (GEN), administered alone or in combination, and investigated the underlying molecular mechanisms using both in vivo and in silico approaches. Our findings demonstrated that co-exposure to PsNPs and GEN induces combined treatment response in liver by triggering oxidative stress, inflammation and apoptosis responses, associated with a dysregulation of genes related to oxidative stress (NRF2), inflammation (TNF-α, IL-1β), and apoptosis (Bax, Bcl-2, caspase-9, and caspase-3). Molecular docking analyses further supported these observations by revealing strong binding affinities of nanoplastics with key proteins involved in oxidative stress and inflammatory pathways. Our results revealed that co-exposure of adult rats to PsNPs and GEN induces an adverse effect on hepatic function. This study provides new evidence on the combined toxicity of polystyrene nanoplastics and pharmaceutical pollutants on liver function, suggesting a potential co-exposure-associated effect interaction between these contaminants.